NSAIDS /certified fixed orthodontic courses by Indian dental academy


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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.

Indian dental academy provides dental crown & Bridge,rotary endodontics,fixed orthodontics,
Dental implants courses.for details pls visit www.indiandentalacademy.com ,or call

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NSAIDS /certified fixed orthodontic courses by Indian dental academy

  1. 1. INDIAN DENTAL ACADEMY Leader in continuing dental education www.indiandentalacademy.com www.indiandentalacademy.com
  4. 4. • IMPORTANCE OF INFLAMMATION • DEFINITION OF INFLAMMATION As per Ebert & Grant “Inflammation is a process that begins following sub lethal injury to tissue and ends with permanent destruction of tissue or with complete healing”. www.indiandentalacademy.com
  5. 5. FUNDAMENTAL EVENTS IN INFLAMMATION 1. Increased permeability of the micro vasculature. 2. Accumulation and activation of Leucocytes. www.indiandentalacademy.com
  6. 6. MEDIATORS OF INFLAMMATORY PROCESS • MAJOR GROUPS  TISSUE  Lymphocyte products  Macrophage products  Mast Cell products • MAJOR MEDIATORS Interferon γ Interleukins Skin reactive factor TNF-α PAF Histamine Cytokines Prostaglandin D2 www.indiandentalacademy.com
  7. 7.  Eosinophil Products • PLASMA  Kinin System  Complement System  Clotting System • Lysosomal Enzymes • Major Basic proteins • Leukotrienes Bradykinin C3 fragments C5 fragments Fibrinopeptides Fibrin Degradation products www.indiandentalacademy.com
  8. 8. HOW NSAIDS WORKS • Interfering with cycloxygenase pathway • Process begins with AA-a dietary 20 carbon poly unsaturated fatty acid obtained from animal fat • AA is liberated from membrane phospholipids by the action of phospholipase A2. • Free AA is metabolically transformed through either cycloxygenase or lipoxygenase pathway • When AA is enzymatically oxidized by cycloxygenase it forms unstable intermediates(PGG2 and PGH2) leading to prostanoid synthesis • By the action of lipoxygenase,AA forms leukotrienes • This process is referred to as arachidonic acid cascade www.indiandentalacademy.com
  9. 9. ARACHIDONIC ACID Lipooxygenase Leukotrienes Bronchospasm Inflammation COX-1 Prostaglandin Gastric protection uterine contraction, renal function Tissue damage COX-2 Throboxanes prostaglandins Platelet Aggregation www.indiandentalacademy.com Pain inflammation, renal function
  10. 10. www.indiandentalacademy.com
  11. 11. www.indiandentalacademy.com
  12. 12. Cox-1 And Cox-2 • Cox-1(constitutive) “-House keeping” function - For blood clotting - For kidney function - For stomach protection • Cox-2 (induced) contributes: - Pain - Heat www.indiandentalacademy.com - Swelling
  13. 13. CLASSIFICATION OF NSAIDS A. ANALGESIC AND ANTI – INFLAMMATORY 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. Salicylates : Aspirin, Salicylamide, Diflunisal. Pyrazolone : Phenylbutazone, Oxyphenbutazone. Indole Derivatives : Indomethacin,Sulindac. Propionic acid derivatives : Ibuprofen,Naproxen, Ketoprofen, Fenoprofen. Anthranilic Acid derivative : Mephenamic acid. Aryl – acetic acid derivative : Diclofenac,Tolmetin. Oxicam derivative : Piroxicam, Tenoxicam, Meloxicam. Pyrrolo – Pyrrole derivative : Ketorolac. Sulfonanilide derivative : Nimesulide. www.indiandentalacademy.com Alkanones : Nabumetone.
  14. 14. B. ANALGESIC BUT POOR ANTIINFLAMMATORY 1. Para- aminophenol derivative : Paracetamol (Acetaminophen). 2. Pyrazolone derivative : Metamizol (Dipyrone) propiphenazone. 3. Benzoxazocine derivative : Nefopam. www.indiandentalacademy.com
  15. 15. SALICYLATES  ASPIRIN ACTIONS:- 1 i. Analgesic, Anti- pyretic and Anti-inflammatory. ii. Weaker analgesic than morphine type drugs. iii. Analgesic action is mainly due to obtunding of peripheral pain receptors and prevention of PG mediated sensitization of nerve endings. iv. It resets the hypothalamic thermostat and rapidly reduces fever by promoting heat loss but does not decrease heat production. www.indiandentalacademy.com
  16. 16. 2. Aspirin and released Salicylic acid irritates gastric mucosa – causes epigastric distress, nausea, vomiting. 3. It interferes with platelet aggregation and bleeding time is prolonged to nearly twice the normal. - Absorbed from stomach and small intestine. - Slowly enters brain and freely crosses placenta. www.indiandentalacademy.com
  17. 17. Effects of NSAIDS on upper GIT www.indiandentalacademy.com
  18. 18. Contraindications to the use of Aspirin and other salicylates: • Disease state 1 Ulcer 2 Asthama 3 Diabetes Possible adverse effect Internal Bleeding,possible hemorrhage Asthmatic attack resembling allergic reaction. low doses may cause hyperglycemia . high doses may cause www.indiandentalacademy.com hypoglycemia.
  19. 19. Adverse effects: 1. Analgesic dose – nausea, vomiting, epigastric distress and increased blood loss in stools. 2. Hypersensitivity and Idiosyncrasy. 3. Inflammatory doses- produce syndrome called ‘ Salicylism’ . 4. Acute Salicylate poisoning more common in children causes vomiting, dehydration , electrolyte imbalance, delirium, hallucinations,convulsions, and death. www.indiandentalacademy.com
  20. 20. USES 1. Analgesic- for headache, backache, myalgia, joint pain, neuralgias,etc.low dose .3 to .6 gm sixth hourly. 2. Antipyretic- effective in fever of any origin. 3. Acute rheumatic fever- It is the first drug to be used in all cases. 4. Rheumatoid arthritis- It is the first drug to be tried.Produces relief of pain, swelling, and morning stiffness. 5. Other conditions: Osteoarthritis, post myocardial infarction and post stroke patients. www.indiandentalacademy.com
  21. 21. Precautions: • Should be stopped a week before elective surgery. • Should be avoided during pregnancy, lactation. • Should be avoided in chronic liver diseases and in patients with bleeding tendencies. www.indiandentalacademy.com
  22. 22. Pyrazolones: • Phenylbutazones: 1. Inhibits Cox and is more potent Anti inflammatory. 2. Analgesic and anti-pyretic effect ois poor and slower in onset. 3. Causes definite retention of Na and water by direct action on renal tubules-edema,which occurs after 1-2weeks of use. 4. Completely absorbed orally and completely metabolised in liver. www.indiandentalacademy.com
  23. 23. Adverse effects; More toxic than Aspirin • Nausea,vomitting,epigastric distress, and epigastric ulceration are common. • edema is a major limitation for use for more than 1-2 weeks. • Hypersensitivity reactions like rashes,serum sickness and stomatitis. • Bone marrow depression, agranulocytosis and Steven-Johnsons syndrome are more serious. www.indiandentalacademy.com
  24. 24. Indole derivatives: • Indomethacin: • Water insoluble , and soluble in common organic slovents. • Actions: Analgesic and potent anti-inflamatory and anti pyretic action. inhibits PG synthesis as well as phospho- diesterase thus increasing cyclic AMP intracellularly. Also interferes with migration of leukocytes to inflammatory cells Absorbed orally reaching peak plasma levels in one and half hours. www.indiandentalacademy.com
  25. 25. Clinical use: • • • • • Rheumatoid Arthritis and associated disorders. Ankylosing spondylitis. Gout. Neurovascular headache. Malignancy associated fever refractory to other anti-pyretic. • Most commonly used drug for closure for closure of PDA. www.indiandentalacademy.com
  26. 26. Propionic Acid Derivatives: Ibuprofen: • Actions similar to Aspirin but are better tolerated orally although they may produce gastric irritation and ulceration. • Highly bound to plasma protiens- 90 –99% • Metabolised in liver. www.indiandentalacademy.com
  27. 27. Interactions/Contraindications 1 should be avoided with anti-coagulants as they inhibit platelet funtions 2 Not to be prescribed during pregnancy and peptic ulcer patients. 3 Contra indicated in indivisuals with nasal polyps, angioedema and bronchospasmic activity to aspirin. www.indiandentalacademy.com
  28. 28. Anthranilic Acid derivative: Mefenamic acid • Actions: weaker analgesic than aspirin. • Inhibits PG synthesis. • Exerts peripheral as well as central analgesic activity. www.indiandentalacademy.com
  29. 29. Clinical use: • Dull aching pain. • Indicated primarily as an analgesic in muscle,joint and soft tissue pain-where strong anti-inflammatory action is not needed. www.indiandentalacademy.com
  30. 30. Adverse effects • Nausea,vomitting,epigastric distress, and epigastric ulceration are common. • Dizziness,headache,skin rashes,heamolytic anemia and blood dyscrasias. www.indiandentalacademy.com
  31. 31. ArylAcetic acid derivatives: Diclofenac,Tolmetin • Actions: • Newer analgesics and antipyretic and antiinflammatory drug. • Inhibits PG synthesis and short lasting antiplatelet action. • Concentration in synovial fluid is three times more than in plasma. • Well absorbed orally. • Plasma t1/2-2hrs www.indiandentalacademy.com
  32. 32. Clinical use: • Osteoarthritis,Rheumatoid arthritis,ankylosing spondylitis,bursitis. • Post traumatic and post-op inflammatory conditions-affords quick relief of pain and wound edema. www.indiandentalacademy.com
  33. 33. Oxicam derivatives piroxicam • Actions: • lowers PG concentrations in synovial fluid. • Produces ratio of T-helper to T-supressor lymphocytes. • Inhibits platelet aggregation thus prolongs bleeding time. • Half life-28-45hrs. www.indiandentalacademy.com
  34. 34. Pyrolo-pyrrole derivatives ketorolac: • Actions; • Highly potent member of a new class of analgesic compound. • Has both anti-inflammatory and anlgesic property but is more systemic analgesic then anti-inflammatory. • More potent than indomethacin andphenylbutazone. • Inhibits PG synthesis and is believed to relieve pain by peripheral mechanism. • In post-op pain it has equal efficacy of morphine. • Excreted in urine-90% unchanged. www.indiandentalacademy.com
  35. 35. Uses: • Frequently used in post op and acute musculo-skeletal pain • May also be used for renal colic, migraine and pain due to bone metastasis. • Should not be given in patients on anticoagulants. www.indiandentalacademy.com
  36. 36. Sulfonanilide derivatives: nimesulide: • Selective for Cox-2. • Can be given for asthamatics. • Newer NSAID and is a relatively weaker inhibitor of PG synthesis. • Completely absorbed orally and is excreted in urine. www.indiandentalacademy.com
  37. 37. Uses: • Primarily in short lasting painful inflammatory conditions like sport injuries,sinusitis,other ENT disorders,dental surgeries,bursitis,low back ache and post op pain. • Nimesulide is safe (Hindustan Times-13th Jan 2003) www.indiandentalacademy.com
  38. 38. ParaAminoPhenol derivatives paracetamol(acetaminophen) • Action: • Central analgesic action is similar to Aspirin but negligible anti-inflammatory action. • Good and promptly acting anti-pyretic. • Doest not affect platelet function. • No effect on CVS,and rare gastric irritation. • Well absorbed orally,uniformly distributed in body and excreted rapidly in urine. • Plasma t1/2- 2-3hrs. www.indiandentalacademy.com
  39. 39. Adverse effects: • In isolated anti-pyretic doses , it is safe and well tolerated. • Nausea and rashes occur rarely. • Analgesic nephopathy occurs after years of heavy ingestion of the drug. • Acute paracetamol can occur specially in small children who have low hepatic glucoronide conjugating ability. www.indiandentalacademy.com
  40. 40. Acute Paracetamol poisoning • Occurs if a large dose of more than 150mg/kg is taken. • Fatality is common with more than 250mg/kg. • Early manifestations are nausea,vommiting, abdominal pain and liver tenderness with no impairment of conciousness. • After 12-18hrs centri-lobular hepatic necrosis occurs. • Hypoglycemia may progress to coma.] • Jaundice occurs after 2 days. www.indiandentalacademy.com
  41. 41. Treatment: • If patient is brought early, vomiting should be induced or gastric lavage done. • Activated charcoal is given orally or through tube to prevent further absorption. • Specific: N-Acetyl Cysteine 150mg/kg should be infused iv over 15mins followed by the same dose iv over the next 20hrs. www.indiandentalacademy.com
  42. 42. www.indiandentalacademy.com
  43. 43. SELECTIVE COX2 INHIBITORS • First generation - Celecoxib and rofecoxib • Second generation - Valdecoxib www.indiandentalacademy.com
  44. 44. CELECOXIB • First selective cox2 inhibitor to be approved by FDA • Launched in 1999 • Exerts potent anti inflammatory analgesic and anti-pyretic action with low ulcerogenic potential • Time action and peak analgesic effort is approx. half than that of ibuprofen 600mg. www.indiandentalacademy.com
  45. 45. ADVERSE EFFECTS • Mild diarrhoea • Abdominal pain • Dyspepsia DOSAGE 100-200mg BD www.indiandentalacademy.com
  46. 46. • Celecoxib is effective for cancer prevention in people with familial adenomatous polyposis • Celecoxib is the only drug that is approved by USA-FDA for the treatment of familial adenomatous polyposis www.indiandentalacademy.com
  47. 47. • Rofecoxib-selective cox2 inhibitor • Reported to be more selective cox2 inhibitor than celecoxib using in-vitro assays • Greater analgesic effect than celecoxib • 800 times more selective for cox2 than cox1 • Half life 17 hr DOSAGE • 50 mg OD www.indiandentalacademy.com
  48. 48. • VALDECOXIB • Has quicker action than rofecoxib • Administration of valdecoxib resulted in better pain relief and lower pain intensity as compared to rofecoxib • DOSAGE • 20mg BD www.indiandentalacademy.com
  49. 49. DRUGS IN THE PIPELINE • PARECOXIB - An injectable product of valdecoxib used for managing severe acute pain including post op pain -Parecoxib 40mg and 80 mg is effective and safe for treating post op pain ETORICOXIB - Currently being reviewed by FDA - Highly selective for cox2 www.indiandentalacademy.com
  50. 50. REFERENCES • Essentials of medical pharmacology fourth edition K.D.TRIPATHI • Principles of medical pharmacology fifth edition KALANT • Pharmacology-fourth edition DALE,RANG AND RITTER • Basic and clinical pharmacology BERTRAN AND KATZUNG • Dental therapeutic update october 2002 www.indiandentalacademy.com
  51. 51. THANK YOU www.indiandentalacademy.com